Weiya Ma
M.D., Ph.D.

Weiya Ma

E-2107, Pavillon Perry

6875 Boulevard LaSalle
Montréal, QC
H4H 1R3

(514) 761-6131 x2935

(514) 762-3034

Champs de recherche: 
Neurosciences fondamentales / Recherche animale

Thème de recherche: 
Stress, désordres de l'humeur et de l'impulsivité

Chercheure, Centre de recherche Douglas
Professeure adjointe, Département de psychiatrie, Université McGill

Chronic pain mechanisms

Chronic pain is a serious clinical concern which affects more than 20% of the world population and imposes heavy financial burdens on the health care systems. Chronic pain is also a major cause for depression and suicide. Chronic pain conditions usually include inflammatory pain (e.g. arthritis and migraine) and neuropathic pain (e.g. post-herpetic neuropathy, diabetic neuropathy and trigeminal neuralgia). The treatments of chronic pain are frequently unsatisfactory due to unclear key mechanisms. However, sensitization of neurons located along pain transmission pathway (peripheral and central sensitization) by pro-inflammatory mediators is strongly implicated as the mechanisms underlying the development of chronic pain. The research in my lab focuses on the plastic events occurring in the nociceptive dorsal root ganglion (DRG) neurons (nociceptors) during inflammatory pain, neuropathic pain and prolonged sensitization pain. These plastic events underlie the long lasting peripheral sensitization and contribute to the transition from acute to chronic pain. More specifically, we are interested to explore the chronic sensitizing effects of PGE2 on DRG neurons, such as PGE2-facilitated cell surface trafficking and synthesis of various pain mediators. To address our research questions, we are applying behavioral, pharmacological, morphological, neurochemical and molecular biological approaches in both in vivo and in vitro models.

I. Articles

1. St-Jacques, B. and Ma, W. Peripheral prostaglandin E2 prolongs the sensitization of nociceptive dorsal root ganglion neurons possibly by facilitating the synthesis and anterograde axonal trafficking of EP4 receptors. Exp Neurol. 261:354-366, 2014.

2. W. Ma and R Quirion Targeting cell surface trafficking of pain-facilitating receptors to treat chronic pain conditions. Expert Opin Ther Targets. 18(4):459-72, 2014

3. M.Shukla, R.Quirion and W.Ma Reduced expression of pain mediators and pain sensitivity in amyloid precursor protein over-expressing CRND8 transgenic mice. Neuroscience, 250:92-101, 2013.

4. B. St-Jacques and Ma, W. Prostaglandin E2/EP4 signaling facilitates EP4 receptor externalization in primary sensory neurons in vitro and in vivo. Pain, 154:313–323, 2013.

5. W. Ma Targeting trafficking of nociceptive receptors to treat chronic pain conditions. J. Autacoids, 1:2, 2012

6. W.Ma, B.St-Jacques and P. Cruz Duarte Targeting the facilitating effects of injured nerve-derived PGE2 on the synthesis of pain mediators in primary sensory neurons to treat neuropathic pain. Expert Opin Ther Targets, 16(6):527-40, 2012.

7. P. Cruz Duarte, B. St-Jacques and W.Ma Prostaglandin E2 contributes to the synthesis of brain-derived neurotrophic factor in primary sensory neuron in ganglion explant cultures and in a neuropathic pain model . Exp. Neurol., 234 (2): 466-481, 2012.

8. B. St-Jacques and W. Ma Role of prostaglandin E2 in the synthesis of the pro-inflammatory cytokine interleukin-6 in dorsal root ganglion neurons: an in vivo and in vitro study. J. Neurochem. 118(5):841-854, 2011.

9. Y. Hong, D.Wang, J-G, Chabot, W. Ma, P.Chen, and R. Quirion A Role for Protein Kinase C-Dependent Upregulation of Adrenomedullin in the Development of Morphine Tolerance in Male Rats. J.Neurosci. 30(37):12508-12516, 2010.

10. Wang Z, Ma W, Chabot JG, Quirion R Morphological evidence for the involvement of microglial p38 activation in CGRP-associated development of morphine antinociceptive tolerance. Peptides, 31(12):2179-84, 2010

11. Wang Z, Ma W, Chabot JG, Quirion R. Calcitonin gene-related peptide as a regulator of neuronal CaMKII-CREB, microglial p38-NFkappaB and astroglial ERK-Stat1/3 cascades mediating the development of tolerance to morphine-induced analgesia. Pain, 151(1):194-205 , 2010.

12. Ma,W. Chronic PGE2 treatment induces the synthesis of the pain-related peptides substance P and calcitonin gene-related peptide in cultured sensory ganglion explants. J.Neurochem., 115(2):363-72 , 2010.

13. Ma,W., Y.Dumont, F.G. Vercauteren and R. Quirion Lipopolysaccharide induces calcitonin gene-related peptide in the RAW 264.7 macrophage cell line. Immunology, 130(3):399-409, 2010.

14. Ma,W., J-G.Chabot, F.Vercauteren and R.Quirion Injured nerve-derived PGE2 contributes to the maintenance of neuropathic pain in aged rats. Neurobiology of Aging, 31(7):1227-37, 2010.

15. Z.Wang, W. Ma, J-G.Chabot and R.Quirion Cell type specific p38 and ERK activation differentially mediates CGRP involvement in the development of tolerance to morphine-induced analgesia. FASEB Journal, 23(8):2576-86, 2009.

II. Book Chapters

1. W. Ma PGE2 induced nociceptor sensitization and potentiation contribute to chronic pain conditions. An invited book chapter in Nociceptors: Neurobiology, Functional Properties and Role in Pain Processing. Nova Science Publisher, Inc., New York, 2015, in press.

2. W. Ma and R. Quirion Role of COX2/PGE2/EP Receptor Signaling In Neuropathic Pain. An invited book chapter in Horizons in Neuroscience Research. Volume 13, pp1-36, Eds. Andres Costa and Eugenio Villalba, Nova Science Publisher, Inc., New York, 2014.

3. W. Ma and R. Quirion Role of protein kinase B (PKB)/Akt signaling in nociception and chronic pain conditions. An invited book chapter In Advances in Medicine and Biology. Volume 62, pp83-104, Eds. Leon V. Berhardt, Nova Science Publisher, Inc., New York, 2013.

4. Y. Hong, J-G. Chabot, W. Ma, P. Chen and R. Quirion Adrenomedullin- a novel pain peptide involved in tolerance to the antinociceptive effect of opiates. Proceeding of International Conference on neuropeptides, 2009, in press.

5. Ma, W, J-G. Chabot, A.Schorscher-Petcu, Y.Hong, Z.Wang and R. Quirion. CGRP and adremomedullin as pain related peptides. In The calcitonin gene-related peptide family: Form,Function and Future Perspective. Chapter 10, Eds. D.L.Hay and I.M.Dickerson, Springer, Netherland 2008, pp.151-171.

6. Ma, W, J-G. Chabot and R. Quirion Calcitonin gene-related peptide and receptors. New Encyclopedia of Neuroscience, Elsevier Reference Book. Pages 509-520, 2007.

7. Ma, W Involvement of macrophage derived prostaglandins in the pathogenesis of neuropathic pain caused by nerve injury. In Progress in Inflammation Research, Chapter II, pp39-94, Eds. J.A.Pitzer, Nova Science Publisher, Inc., New York, 2006.

Weiya Ma completed her Ph.D. from Dept. of Pharmacology and Therapeutics at McGill University, Canada in 90’s. After finishing her postdoctoral fellowship in Canada, she went to Wake Forest University in States to take a faculty position in Dept. of Anesthesiology. Then she moved back Canada to continue her research at Douglas Mental Health University Institute. Now she is an assistant professor at Dept. of Psychiatry, McGill University. Thus far she has published more than 70 research articles and numerous book chapters in the pain research field. Her novel studies unraveled the role of pain-related neuropeptides such as substance P, calcitonin gene-related peptide and adrenomedullin in nociception, neuropathic pain and morphine tolerance. Her pioneer work exploring the role of inflammatory mediator prostaglandin E2 in the genesis of chronic pain has let her become a leader in this field. Her research publications have been widely cited (citations: 3226 and h-index: 36). She was frequently invited to present her work at seminars, to contribute review articles and book chapters to introduce her research works. Her research has been supported by Canadian Institutes of Health Research, Natural Sciences and Research Council of Canada and Louise and Alan Edwards Foundation in Pain Research. Email: Weiya.ma@douglas.mcgill.ca; Weiya.ma2@mcgill.ca

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